Cryptolepis buchanani Roem. & Schult. (Family Asclepiadaceae) is distributed throughout hot deciduous forests of India and holds a very prestigious position in Ayurveda.
It is a very useful plant because of its multiple uses as a traditional medicine, such as anti-diarrheal, anti-bacterial, anti-ulcerative, anti-inflammatory, blood purifier and for lactation in women [Bhakuni, D. S., Dhar, M. L., Dhar, M. M., Dhawan, B. N., and Mehrotra, B. N., Ind. J. Expt. Biol., 7: 250-262 (1969), Bhav Prakash, Commentary on Bhav Prakash Nighantu edited by C. K. Chunekar, Chowkhamba Vidya Bhavan, Varanasi 4th edition: 427 (1969)].
Ethanolic extract of roots and stem show hypotensive, central nervous system depressant and antiamphetaminic activity [Joshi, M. C., Patel, M. B. and Mehta, P. J. Bull. Med. Ethno. Bot. Res., 1: 8-24 (1980)].
Ethanolic extract of aerial parts of plant shows diuretic activity [Dhawan, B. N., Patnaik, G. K., Rastogi, R. P., Singh, K. K. and Tandon, J. S., Ind. J. Expt. Biol.,15: 208-219 (1977)].
Root bark is used in rheumatic pains [Mudgal, V. and Pal, D. C., Bull. Bot. Surv. Ind., 22: 59-62 (1980)].
Stem constituents are alkaloids and triterpenes, leaves constituents are α and β amyrin (Asolkar, L. V., Kakkar, K. K. and Chakre, O. J., Glossary of Indian Medicinal Plants with active principles, part-1, A-K., 1965-1981(1992)] and cryptolepine—the methyl-quinolanol alkaloid of cryptolepis sanguinolenta. Pyridine alkaloid, buchanine [Dutta, Sunil K, Sharma, Batuk N, Sharma, Priya V. Phytochemistry 17, 2047(1978)] and a cardenolide cryptosin, 7,8-Epoxy-3,11,14-trihydroxy-12-Oxocard 20 (22)-enolide [Venkateshwara R; Narendra N; Viswametra M. A; Vaidyanathan C. S.; Phytochemistry 28, 1203 (1989)] are the major chemical constituent of the plant. Apart from these chemical constituents cryptanoside-A to D and germenicol [Purshothman K. K; Saradha V; Connolly J. D; Rycroft D. S, Rev. Latinomer Quim., 19, 28 (1988)], 1,3,6-trinicotinoyl-β-D-glucopyranoside and 1,3,6-trinicotinoyl-α-D-glucopyranoside, n-trinicontanol, n-triactonoic acid, β-amyrin and β-sitosterol glucoside [Dutta S. K; Sharma B. N; Sharma P. V., Phytochemistry, 17, 2047 (1978), Dutta S. K; Sharma B. N, Sharma P. V; (1980) Phytochemistry, 19, 1278 (1980)].
The alcoholic extract of the root shows the presence of sterols, reducing sugars and traces of glycosides and exhibited antiplatelet effects in vitro in humans, rabbits and rats. In rats, it exhibited ADP-aggregation in vitro with delayed onset and prolonged action. It exhibited an indirect fibrinolytic action in the rat possibly by causing the release of plasminogen activators from the vascular endothelium [Oyekan, A. O., Botting, J. H. and Noamesi, B. K., General Pharmacol., 19: 223-227 (1988)].
Liver has a pivotal role in regulation of physiological processes. Toxic chemicals and infections mainly cause liver diseases. Hepatocyte alterations of various origins result in acute and chronic dysfunctions, which may be lethal [Decker K. and Keppler D. Rev. Physiol. Biochem. Pharmacol., 71, 79-106 (1974)].
Liver disorders are still the major hazard both in urban and rural population. Despite scientific advances in our understanding in the management of liver disorders and the leads provided by traditional system of medicine, no specific treatment for liver ailments is available except a few herbal preparations, WHO, Regional Office Manila, 1993.; [Subeamoniam and Pushpangadan, Indian Journal of Pharmacology, 31,166-175 (1999)].
It is emphasized that hepatotoxin that causes acute hepatitis should have close resemblance with the viral hepatitis, clinically, biochemically and histologically. In many instances drug induced hepatitis proves indistinguishable from viral hepatitis. Chemically induced hepatic injury for experimental studies should be severe enough to cause death or to modify hepatic function. The mechanism of acute hepatic injury depends upon the chemical compound and the species of animals used. Many chemicals produce parenchymal damage (cytotoxic injury), arrest bile flow and cause jaundice. The damage may be acquired or toxicological phenonmenon, therapeutic misadventure or induced experimentally. Drugs also cause chronic hepatic diseases such as hepatitis, fatty liver, cirrhosis, and several vascular lesions of the liver.
It is the role of hepatoprotective agents to interfere with these pathological processes by blocking their evolution and helping recovery by preventing hepatocytes degeneration, necrosis, steatosis and inflammation, stimulate regeneration processes, and inhibit fibrosis which leads to cirrhosis and death [Doreswamy, R., Sharma, D., Indian Drugs, 32, 139-144 (1995)], Kumar et al, Cell injury and adaptation. In: “Basic Pathology”, 5th. Edn. Prime Books (pvt.) Ltd., Banglore, India. 1992, pp. 3-24.
Acute hepatitis closely resembling viral hepatitis clinically, biochemically and histologically, can be produced by chemicals and drugs in humans and experimental animals, [AL-Tuwaijiri A. et al Heptology, 51: 107-113 (1981); Decker K. and Keppler D. Rev Physiol. Biochem. Pharmacol., 71, 79-106 (1974); Kumar et al, Cell injury and adaptation. In: “Basic Pathology”, 5th. Edn. Prime Books (Pvt.) Ltd., Banglore, India. 1992, pp. 3-24].